新型氧化锆基质标记材料研发成功

近日，中国科学院大连化物所袁景利等人在纳米稀土荧光生物标记材料的制备与生化分析应用研究工作中，成功地研制出一系列粒径在25～55nm的硅胶基质搀杂型纳米稀土荧光生物标记材料、表面带有活性氨基的搀杂型(或共价键合型)纳米稀土荧光生物标记材料及氧化锆基质的搀杂型纳米稀土荧光生物标记材料。     

生物标记用发光材料研究现状

综述了生物标记用发光材料研究进展及其应用现状,对各种材料的特点进行了分析,指出以绿色荧光蛋白等为代表的荧光材料将是未来生物标记的主流.     

福建物构所稀土上转换荧光生物标记材料研究取得新进展

正与传统的分子荧光标记材料(如荧光染料)相比,稀土上转换纳米发光材料不仅化学稳定性高、荧光寿命长、潜在生物毒性低,而且由于采用近红外光源激发具有较大的光穿透深度、无生物组织自荧光以及对生物组织几乎无损伤等显著优点,在荧光生物检测和成像等领域具有重要的应用前景。目前上转换纳米荧光标记材料发展的瓶颈问题是其量子产率低。提高上转换发光效率、探索新型高效的上转换纳米荧光标记材料一直是人们关注的焦点与努力的目标,也是该类材料能否获得实际应用的关键。在国家自然科学基金杰出青年和促进海峡两岸科技合作联合基金、科技部863计划和重大科学仪器开     

两种铀配合物对生物分子的荧光标记性质研究

选用2种铀配合物分别与4种典型的生物分子多巴胺(DA)、抗坏血酸(AA)、尿酸(UA)和牛血清白蛋白(BSA)相互作用,采用荧光分光光度计进行荧光标记性质测试,研究铀配合物对4种生物分子的荧光标记性质。结果表明,4种生物分子对铀配合物的荧光发光产生了一定影响,在不同浓度梯度的生物分子中,浓度越大对铀配合物荧光强度的影响也越大;随着生物分子浓度的增大,出现了荧光猝灭现象,这2种铀配合物可以作为生物分子的荧光探针。为铀配合物在生物分子荧光标记研究方面的应用提供了一定的依据。     

用于生物标记的半导体量子点研究

半导体量子点的独特光学性质使之成为理想的荧光探针材料，在生物医学领域具有广阔的应用前景．本文评述了目前量子点合成、表面修饰、结合生物分子的方法，以及半导体量子点在生物标记应用中相对于传统有机染料的优点．     

阳离子碳点的合成及其对细菌的快速标记成像

碳点是一种强荧光、高稳定性的荧光纳米材料,在生物标记与成像领域具有较大的应用潜力。本研究合成了一种阳离子型的荧光碳点,碳点在紫外激发下发出黄色荧光。将碳点与大肠杆菌混合后,阳离子碳点可以直接作用于大肠杆菌而使大肠杆菌标记上荧光,并可以在荧光显微镜下荧光成像。进一步的研究证明该阳离子碳点也可以对枯草芽孢杆菌、阿氏芽孢杆菌等其他细菌标记和荧光成像,具备发展成为一种快速标记细菌的通用荧光染料的潜力。     

技术贸易

<正>新型纳米晶荧光材料及其应用技术一、项目简介北京理工大学材料学院纳米光子学材料与技术实验室在致力于开发性能优异、绿色、实用的纳米晶发光材料研究。在国家973计划项目和自然基金项目的支持下,研制出一种基于铜铟硫(CuInS_2)和铜铟硒(CuInSe_2)的新型、绿色、低毒荧光纳米晶材料,已在白光照明、发光二极管、生物标记、太阳能电池     

荧光碳纳米粒子的制备及其在细胞标记中的应用

在生物医学领域,对细胞、生物分子进行染色、修饰标记和检测一直是生物医学分析的重要内容.近年来,纳米材料与生物检测技术的结合,使得生物分子的检测有了重要的发展.用30%H2O2/ACOH(V∶V=2∶1)混合氧化性酸溶液回流蜡烛烟炱制备得到荧光碳纳米粒子,用不同浓度的荧光碳纳米粒子对Hela细胞进行荧光标记,在激光共聚焦...     

一种氧杂蒽染料的合成及在水中的光谱性能研究

通过酸催化的缩合反应合成了一种荧烷染料2,研究了其在不同溶剂中的光谱行为。对化合物2的游离氨基进行酰化,得到了新型的荧光染料3。利用核磁共振波谱、高分辨质谱对3进行了结构表征。考察了化合物3在不同的p H水溶液的紫外吸收和荧光光谱变化。研究表明,该化合物在生理p H范围内保持螺环内酯开启状态,并保持较稳定的荧光强度,有作为生物标记及生物成像材料的潜力。     

蛴螬多糖的荧光标记研究

用荧光物质8-氨基-1,3,6奈三磺酸二钠盐(ANTS)对蛴螬活性多糖进行荧光标记,对反应时间、温度、pH值、ANTS浓度进行了单因素考察,采用UV-Vis、Flu、HPGFC等方法对标记结果进行确证。结果表明,蛴螬多糖荧光标记的最佳条件是pH值为5.5,40℃条件下反应20h时反应率最高,其荧光取代度为1.56%。实现了荧光检测器检测或追踪多糖,为多糖的生物机制研究及药代动力学的研究提供一定思路。     

污泥生物炭中氮硫行为及环境效应研究进展

污泥生物炭中氮硫元素含量高,其氮硫行为和环境效应对全球气候变化的影响不容忽视。以往的研究中,研究者往往以富碳生物炭作为主要研究对象,关注碳对全球气候变化的行为和功效,而对氮硫元素的作用关注不够。本文从原始污泥基本性质到其热解过程,再到生物炭的老化,逐步对污泥生物炭整个生命周期内氮硫的行为及其环境效应研究进行综述,并对未来应注重开展的研究方向进行展望,为生物炭中氮硫元素固定、释放及与之关联的环境效应和温室气体排放控制研究提供理论基础。分析表明,污泥中氮元素含量普遍高于硫元素,且热解过程中氮比硫更容易转移至气相产物。氮硫元素随热解温度的增加,在三相产物中的分配都是炭中持续减少,油中先增后减,气中一直增加。高温（＞800℃）条件下,气相中的氮含量高于固相,而硫元素则仍然主要存在于固相中。污泥生物炭老化及其环境效应研究表明,污泥生物炭氮硫元素与土壤的相互作用及其温室效应问题在今后的研究中应引起重视。     

Sp7 Transgenic Mice with a Markedly Impaired Lacunocanalicular Network Induced Sost and Reduced Bone Mass by Unloading

The relationship of lacunocanalicular network structure and mechanoresponse has not been well studied. The lacunocanalicular structures differed in the compression and tension sides, in the regions, and in genders in wild-type femoral cortical bone. The overexpression of Sp7 in osteoblasts resulted in thin and porous cortical bone with increased osteoclasts and apoptotic osteocytes, and the number of canaliculi was half of that in the wild-type mice, leading to a markedly impaired lacunocanalicular network. To investigate the response to unloading, we performed tail suspension. Unloading reduced trabecular and cortical bone in the Sp7 transgenic mice due to reduced bone formation. Sost-positive osteocytes increased by unloading on the compression side, but not on the tension side of cortical bone in the wild-type femurs. However, these differential responses were lost in the Sp7 transgenic femurs. Serum Sost increased in the Sp7 transgenic mice, but not in the wild-type mice. Unloading reduced the Col1a1 and Bglap/Bglap2 expression in the Sp7 transgenic mice but not the wild-type mice. Thus, Sp7 transgenic mice with the impaired lacunocanalicular network induced Sost expression by unloading but lost the differential regulation in the compression and tension sides, and the mice failed to restore bone formation during unloading, implicating the relationship of lacunocanalicular network structure and the regulation of bone formation in mechanoresponse.     

Possible Role of Crystal-Bearing Cells in Tomato Fertility and Formation of Seedless Fruits

Crystal-bearing cells or idioblasts, which deposit calcium oxalate, are located in various tissues and organs of many plant species. The functional significance of their formation is currently unclear. Idioblasts in the leaf parenchyma and the development of crystal-bearing cells in the anther tissues of transgenic tomato plants (Solanum lycopersicon L.), expressing the heterologous FeSOD gene and which showed a decrease in fertility, were studied by transmission and scanning electron microscopy. The amount of calcium oxalate crystals was found to increase significantly in the transgenic plants compared to the wild type (WT) ones in idioblasts and crystal-bearing cells of the upper part of the anther. At the same time, changes in the size and shape of the crystals and their location in anther organs were noted. It seems that the interruption in the break of the anther stomium in transgenic plants was associated with the formation and cell death regulation of a specialized group of crystal-bearing cells. This disturbance caused an increase in the pool of these cells and their localization in the upper part of the anther, where rupture is initiated. Perturbations were also noted in the lower part of the anther in transgenic plants, where the amount of calcium oxalate crystals in crystal-bearing cells was reduced that was accompanied by disturbances in the morphology of pollen grains. Thus, the induction of the formation of crystal-bearing cells and calcium oxalate crystals can have multidirectional effects, contributing to the regulation of oxalate metabolism in the generative and vegetative organs and preventing fertility when the ROS balance changes, in particular, during oxidative stresses accompanying most abiotic and biotic environmental factors.     

Early Life Events and Maturation of the Dentate Gyrus: Implications for Neurons and Glial Cells

The dentate gyrus (DG), an important part of the hippocampus, plays a significant role in learning, memory, and emotional behavior. Factors potentially influencing normal development of neurons and glial cells in the DG during its maturation can exert long-lasting effects on brain functions. Early life stress may modify maturation of the DG and induce lifelong alterations in its structure and functioning, underlying brain pathologies in adults. In this paper, maturation of neurons and glial cells (microglia and astrocytes) and the effects of early life events on maturation processes in the DG have been comprehensively reviewed. Early postnatal interventions affecting the DG eventually result in an altered number of granule neurons in the DG, ectopic location of neurons and changes in adult neurogenesis. Adverse events in early life provoke proinflammatory changes in hippocampal glia at cellular and molecular levels immediately after stress exposure. Later, the cellular changes may disappear, though alterations in gene expression pattern persist. Additional stressful events later in life contribute to manifestation of glial changes and behavioral deficits. Alterations in the maturation of neuronal and glial cells induced by early life stress are interdependent and influence the development of neural nets, thus predisposing the brain to the development of cognitive and psychiatric disorders.     

Molecular mechanisms of aging and immune system regulation in Drosophila

Aging is a complex process that involves the accumulation of deleterious changes resulting in overall decline in several vital functions, leading to the progressive deterioration in physiological condition of the organism and eventually causing disease and death. The immune system is the most important host-defense mechanism in humans and is also highly conserved in insects. Extensive research in vertebrates has concluded that aging of the immune function results in increased susceptibility to infectious disease and chronic inflammation. Over the years, interest has grown in studying the molecular interaction between aging and the immune response to pathogenic infections. The fruit fly Drosophila melanogaster is an excellent model system for dissecting the genetic and genomic basis of important biological processes, such as aging and the innate immune system, and deciphering parallel mechanisms in vertebrate animals. Here, we review the recent advances in the identification of key players modulating the relationship between molecular aging networks and immune signal transduction pathways in the fly. Understanding the details of the molecular events involved in aging and immune system regulation will potentially lead to the development of strategies for decreasing the impact of age-related diseases, thus improving human health and life span.     

Streptozotocin-Induced Diabetes Causes Changes in Serotonin-Positive Neurons in the Small Intestine in Pig Model

Serotonin (5-hydroxytryptamine or 5-HT) is an important neurotransmitter of the central and peripheral nervous systems, predominantly secreted in the gastrointestinal tract, especially in the gut. 5-HT is a crucial enteric signaling molecule and is well known for playing a key role in sensory-motor and secretory functions in the gut. Gastroenteropathy is one of the most clinical problems in diabetic patients with frequent episodes of hyperglycemia. Changes in 5-HT expression may mediate gastrointestinal tract disturbances seen in diabetes, such as nausea and diarrhea. Based on the double immunohistochemical staining, this study determined the variability in the population of 5-HT-positive neurons in the porcine small intestinal enteric neurons in the course of streptozotocin-induced diabetes. The results show changes in the number of 5-HT-positive neurons in the examined intestinal sections. The greatest changes were observed in the jejunum, particularly within the myenteric plexus. In the ileum, both de novo 5-HT synthesis in the inner submucosal plexus neurons and an increase in the number of neurons in the outer submucosal plexus were noted. The changes observed in the duodenum were also increasing in nature. The results of the current study confirm the previous observations concerning the involvement of 5-HT in inflammatory processes, and an increase in the number of 5-HT -positive neurons may also be a result of increased concentration of the 5-HT in the gastrointestinal tract wall and affects the motor and secretory processes, which are particularly intense in the small intestines.     

Stress and strain state of concrete during freezing and thawing cycles

The objective of this work is to calculate the pressures, stresses, and strains induced into moist concrete during freezing and thawing. The applied theory is based on thermodynamics and the linear theory of elasticity. If no additional salts are dissolved in the pore water the inputs needed in the theory are relative humidity and temperature measured in the sample chamber and inside concrete and evaporable water amount in the pore structure. Theoretical results were compared with the test results made with two concretes cured under water or at 96% relative humidity. One of the concretes was air entrained and in the comparison concrete no air-entraining agents were used. In the test cylinders cured under water the largest tensional stresses in freezing occurred on the surface of the test cylinders both in the axial and tangential direction. The largest tensional stress was 2.2 MPa, both in air-entrained and in non air-entrained concretes. The largest tensional stresses in the warming phase took place at the end of the thawing period when the chamber temperature was around +5 °C. Then the maximum tension occurred in the middle of the concrete cylinder in the axial direction of the cylinder. This maximum tensional stress was over 2.5 MPa in the air-entrained concrete cured in the relative humidity of 96%. The thermodynamic pumping effect at the end of the thawing phase in every cycle can increase the pore water amount remarkably if free water or moisture is available on the surface of the structure or in the environment vapor. The thermodynamic pumping effect seems to be remarkably greater and more dangerous in air-entrained concretes.     

木质素在超临界甲醇和乙醇溶剂中液化过程分析

通过研究木质素分别在超临界甲醇和乙醇溶剂中的液化过程，分析反应温度（260～340℃）及反应时间（0～120min）对木质素在两种溶剂中的转化率、生物油收率及其组分差异的影响。实验表明，木质素在超临界乙醇中的转化率及产物收率均高于甲醇。当反应温度340℃，反应时间60min，木质素在超临界乙醇中的转化率和生物油收率比在甲醇中分别提高了16.23%和11.54%，残渣收率降低了16.23%。通过GC-MS和FTIR对生物油和残渣分析，发现生物油组分中芳香族化合物相对含量较高，在甲醇和乙醇溶剂中分别达到66.13%和58.84%；随着反应时间的延长，甲醇溶剂中残渣的醚键官能团逐渐增强，而在乙醇溶剂中则先增强后减弱。分析认为在木质素降解过程中，超临界乙醇和甲醇均可产生氢自由基作为供氢体，攻击木质素及其大分子片段中的官能团，同时使液化产物中的活性片段减活，减弱重聚合反应，从而更利于芳烃产物的生成。而甲醇在液化过程中容易与木质素断键产生的苯酚中间体发生脱氢缩合反应，通过醚键聚合产生长链芳香族化合物，形成残渣，降低生物油收率。     

Gender-Related Differences in BMP Expression and Adult Hippocampal Neurogenesis within Joint-Hippocampal Axis in a Rat Model of Rheumatoid Arthritis

BMPs regulate synovial quiescence and adult neurogenesis in the hippocampus in non-stress conditions. However, changes in BMP expression that are induced by inflammation during rheumatoid arthritis (RA) have not yet been reported. Here, we show that signalling with synovial BMPs (BMP-4 and -7) mediates the effect of systemic inflammation on adult neurogenesis in the hippocampus during pristane-induced arthritis (PIA) in Dark Agouti (DA) rats, an animal model of RA. Moreover, we show gender differences in BMP expressions and their antagonists (Noggin and Gremlin) during PIA and their correlations with the clinical course and IL-17A and TNF-α levels in serum. Our results indicate gender differences in the clinical course, where male rats showed earlier onset and earlier recovery but a worse clinical course in the first two phases of the disease (onset and peak), which correlates with the initial increase of serum IL-17A level. The clinical course of the female rats worsened in remission. Their prolonged symptoms could be a reflection of an increased TNF-α level in serum during remission. Synovial inflammation was greater in females in PIA-remission with greater synovial BMP and antagonist expressions. More significant correlations between serum cytokines (IL-17A and TNF-α), and synovial BMPs and their antagonists were found in females than in males. On the other hand, males showed an increase in hippocampal BMP-4 expression during the acute phase, but both genders showed a decrease in antagonist expressions during PIA in general. Both genders showed a decrease in the number of Ki-67⁺ and SOX-2⁺ and DCX⁺ cells and in the ratio of DCX⁺ to Ki67⁺ cells in the dentate gyrus during PIA. However, in PIA remission, females showed a faster increase in the number of Ki67⁺, SOX-2⁺, and DCX⁺ cells and a faster increase in the DCX/Ki67 ratio than males. Both genders showed an increase of hippocampal BMP-7 expression during remission, although males constantly showed greater BMP-7 expression at all time points. Our data show that gender differences exist in the BMP expressions in the periphery–hippocampus axis and in the IL-17A and TNF-α levels in serum, which could imply differences in the mechanisms for the onset and progression of the disease, the clinical course severity, and adult neurogenesis with subsequent neurological complications between genders.     

TrkB Receptor Signalling: Implications in Neurodegenerative,Psychiatric and Proliferative Disorders

The Trk family of receptors play a wide variety of roles in physiological and disease processes in both neuronal and non-neuronal tissues. Amongst these the TrkB receptor in particular has attracted major attention due to its critical role in signalling for brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and neurotrophin-4 (NT4). TrkB signalling is indispensable for the survival, development and synaptic plasticity of several subtypes of neurons in the nervous system. Substantial evidence has emerged over the last decade about the involvement of aberrant TrkB signalling and its compromise in various neuropsychiatric and degenerative conditions. Unusual changes in TrkB signalling pathway have also been observed and implicated in a range of cancers. Variations in TrkB pathway have been observed in obesity and hyperphagia related disorders as well. Both BDNF and TrkB have been shown to play critical roles in the survival of retinal ganglion cells in the retina. The ability to specifically modulate TrkB signalling can be critical in various pathological scenarios associated with this pathway. In this review, we discuss the mechanisms underlying TrkB signalling, disease implications and explore plausible ameliorative or preventive approaches.